Peroneal Spastic Flatfoot Syndrome Due to Fibrosarcoma
JAMES F. RICHARDS, JR., M D.
In January 1970 a 13-year-old white boy was referred to us with the diagnosis of "post-polio" and a history of increasing right lower limb weakness and deficit extending over several years. He reportedly had premature closure of his cranial fontanels but the age of closure was unknown. At the age of three years, the right foot was noted to be one size smaller than the left. At the age of five years, following a head injury without loss of consciousness, the boy began to have vague pain in the right lower extremity. About this time an older brother had documented poliomyelitis.
Examination revealed a well-developed boy, slightly obese, with a considerable limp and apparent shortness of the right lower limb. Results of a physical examination, including head, chest, and abdomen, were normal except for the right lower extremity, where atrophy was noted in the calf and thigh. He also had severe loss of subtalar motion on the right with tenderness in the posterior tibial-peroneal-tendon areas, severe and well localized. He seemed intact neu-rologically and we felt he had "peroneal spastic flatfoot." The patient was placed in a short-leg cast and followed in the Elk's Harry Anna Home for Crippled Children.
X-rays of the foot revealed a radio-dense deposit suggestive of ossification or calcification in the sinus tarsi area (popup1]). There were no obvious bars or bridges as described in the literature and anticipated. The results of a second strength tuberculosis skin test were strongly positive, and it was revealed that the boy had a family history of tuberculosis. Tests for histoplasmosis, coccydio-mycosis and blastomycosis yielded negative results. His chest x-ray did not indicate any tubercular changes.
Some three months after he entered our care the young man was taken to the operating room for biopsy of the right subtalar joint and, perhaps, a triple arthrodesis. Upon entering the sinus tarsi, we found it to be filled with a greyish material resembling granulation tissue. A one-centimeter fragment of white, cheesy material suggestive of caseation was removed. This material could be spooned with a large periosteal elevator or curette. A defect was found in the lateral aspect of the os calcis and this was also curetted. Samples were taken for culture and sensitivities, including acid-fast bacillus studies. The results of these studies were negative. The cartilage was denuded from the subtalar, talonavicular, and calcaneocuboid joints. The wound was closed and the boy was placed in a long-leg cast.
The pathologist was asked to witness the appearance of the gross specimen in the operating room where our initial thought was that this was probably a tuberculous lesion. However, on frozen section the pathology report indicated a very cellular, possibly mitotic, lesion suggestive of fibrosarcoma or synovial
sarcoma ( Fig. 2 ).
The patient was returned from the Orange Memorial Hospital to the Harry Anna Home while we awaited a considered diagnosis from the local pathologist and the Armed Forces Institute of Pathology (AFIP). The boy's wound healed. Some six week postoperative it was the opinion of our local pathologist that this was a pseudosarcomalous fasciitis but the AFIP rendered an opinion that the lesion was sarcoma, possibly the fibrous phase of synovial cell sarcoma, probably fibrosarcoma. The results of full skeletal survey and chest x-ray were normal.
We elected to do a long below-knee amputation with an immediate postoperative fitting. Equal skin flaps were developed at the junction of the middle and distal thirds of the tibia and a myodesis was done using 3.0 Tevdek. The boy did well, the cast was changed at six days, and half the stitches were removed. He received his permanent prosthesis six weeks postamputation.
Examination of the foot revealed a residual lesion within the os calcis consisting of the same material found at biopsy ( Fig. 3 ). When last seen, nine months postamputation, the boy was doing well. His calf muscles were so well developed that he did not need the supracondylar wedge to hold on the prosthesis. We felt this fullness of the triceps surae group was due to the myodesis ( Fig. 4 ).
An interesting aspect of this case is that the typical clinical picture of peroneal spastic flatfoot resulted from the presence of neoplasm. This experience led the author to suggest adding neoplasm to the already well-known list of etiologies of peroneal spastic flatfoot syndrome.1 The list would then read:
PERONEAL SPASTIC FLATFOOT SYNDROME
- Tarso-coalitions with and without accessory ossicles
- Tarso-coalitions with and without associated chondrodystrophy or symphalangism
- Postoperative subtalar arthrodesis
- Tuberculosis of the tarsus
- Rheumatoid arthritis
- Trauma and Sudeck's dystrophy
- Osteoarthritis superimposed on inactive rheumatoid arthritis
- Nonspecific tarsal synovitis
- Occupational strain
A case of peroneal spastic flatfoot syndrome caused by fibrosarcoma of the foot and resulting in a below-knee amputation has been presented.
Co-Chief, Juvenile Amputee Clinic Bureau of Crippled Children Orlando, Florida